ArticleNeurobiology of disease2020
Environmental enrichment prevents Aβ oligomer-induced synaptic dysfunction through mirna-132 and hdac3 signaling pathways.
Article in Neurobiology of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 51 citations in OpenAlex.
- Beta 2-adrenergic pathway combats Alzheimer's disease: Restoring cognition and synaptic integrity.Neural regeneration research · 2026Article
- microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer's disease patients.Acta neuropathologica communications · 2026Article
- Molecular mechanism of Alzheimer's disease using integrated multi-omics.Frontiers in aging neuroscience · 2026Review
- Environmental Enrichment Enhances Visual Function in Adult Amblyopia: Association With miR-132/HDAC3 Regulation.Neural plasticity · 2026Article
- Integrated multi-omics analyses of synaptosomes revealed synapse-associated novel targets in Alzheimer's disease.Molecular psychiatry · 2025Article
- Therapeutic modulation of neurogenesis to improve hippocampal plasticity and cognition in aging and Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Epigenetics of Chronic Stress: Mechanisms and Health Impacts.Current genomics · 2025Review
- NACC2, a molecular effector of miR-132 regulation at the interface between adult neurogenesis and Alzheimer's disease.Scientific reports · 2024Article
- The concept of resilience to Alzheimer's Disease: current definitions and cellular and molecular mechanisms.Molecular neurodegeneration · 2024Review
- Growth-suppressor microRNAs mediate synaptic overgrowth and behavioral deficits in Fragile X mental retardation protein deficiency.iScience · 2024Article
- A bibliometric analysis of studies on environmental enrichment spanning 1967-2024: patterns and trends over the years.Frontiers in behavioral neuroscience · 2024Article
- miRNA-137-5p improves spatial memory and cognition in Alzheimer's mice by targeting ubiquitin-specific peptidase 30.Animal models and experimental medicine · 2023Article
- Activation of βMolecular psychiatry · 2023Article
- Repressor Element-1 Binding Transcription Factor (REST) as a Possible Epigenetic Regulator of Neurodegeneration and MicroRNA-Based Therapeutic Strategies.Molecular neurobiology · 2023Review
- Article
- Dynamic physiological α-synuclein S129 phosphorylation is driven by neuronal activity.NPJ Parkinson's disease · 2023Article
- The Molecular Effects of Environmental Enrichment on Alzheimer's Disease.Molecular neurobiology · 2022Review
- Diverse and Composite Roles of miRNA in Non-Neuronal Cells and Neuronal Synapses in Alzheimer's Disease.Biomolecules · 2022Review
- Multisensory Stimulation Improves Cognition and Behavior in Adult Male Rats Born to LT4-treated Thyroidectomized Dams.Endocrinology · 2022Article
- MicroRNAs and Synaptic Plasticity: From Their Molecular Roles to Response to Therapy.Molecular neurobiology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
As the most common cause of progressive cognitive decline in humans, Alzheimer's disease (AD) has been intensively studied, but the mechanisms underlying its profound synaptic dysfunction remain unclear. Here we confirm that exposing wild-type mice to an enriched environment (EE) facilitates signaling in the hippocampus that promotes long-term potentiation (LTP). Exposing the hippocampus of mice kept in standard housing to soluble Aβ oligomers impairs LTP, but EE can fully prevent this. Mechanistically, the key molecular features of the EE benefit are an upregulation of miRNA-132 and an inhibition of histone deacetylase (HDAC) signaling. Specifically, soluble Aβ oligomers decreased miR-132 expression and increased HDAC3 levels in cultured primary neurons. Further, we provide evidence that HDAC3 is a direct target of miR-132. Overexpressing miR-132 or injecting an HDAC3 inhibitor into mice in standard housing mimics the benefits of EE in enhancing hippocampal LTP and preventing hippocampal impairment by Aβ oligomers in vivo. We conclude that EE enhances hippocampal synaptic plasticity by upregulating miRNA-132 and reducing HDAC3 signaling in a way that counteracts the synaptotoxicity of human Aβ oligomers. Our findings provide a rationale for prolonged exposure to cognitive novelty and/or epigenetic modulation to lessen the progressive effects of Aβ accumulation during human brain aging.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.